The Nitric Oxide hypothesis and the hyperdynamic circulation in cirrhosis

✍ Scribed by Dr. Arieh Bomzon; Laurence M. Blendis

• Publisher: John Wiley and Sons
• Year: 1994
• Tongue: English
• Weight: 988 KB
• Volume: 20
• Category: Article
• ISSN: 0270-9139
• DOI: 10.1002/hep.1840200535

✦ Synopsis

The systemic cardiovascular complications of cirrhosis include generalized vasodilatation manifested clinically as hypotension, decreased systemic vascular resistance, increased cardiac output and an increased rate of blood flow through the tissues (1-4); it is commonly called the hyperdynamic circulation. Preceding these systemic complications are the changes in the splanchnic and, more specifically, the portal circulation. In addition to the increase in portal venous resistance, increase in portal venous inflow is an important factor in the development and maintenance of portal hypertension (5).

Salt and water retention leading to the development of ascites and functional kidney failure or hepatorenal syndrome also occurs in cirrhosis (6). These renal complications are attributed in part to reversible changes in the renal circulation resulting from a decrease in the effective circulating blood volume (i.e., "underfilling") (7, 8). Although others had previously described increases in the circulating blood volume in cirrhotic patients (9, lo), it was not until the late 1960s that Lieberman and Reynolds (11) proposed that sodium retention was associated with expansion of the effective circulating volume (i.e., "overfilling") (12). Levy and his coworkers further fueled the underfilling-vs.-overfilling controversy by providing experimental evidence for overfiIling in the development of the renal complications of cirrhosis (13-18).

In 1988, Schrier and colleagues (19) proposed that the cardiovascular and renal consequences of cirrhosis could